Neville Sanjana
@nevillesanjana.bsky.social
1.1K followers 110 following 87 posts
Scientist at the New York Genome Center & NYU. http://sanjanalab.org
Posts Media Videos Starter Packs
nevillesanjana.bsky.social
Night Science is coming to NYGC!
itaiyanai.bsky.social
NYC Postdocs! Join us for Night Science at the New York Genome Center on June 2nd for a discussion on the creative process of finding novel questions. This time we hit the bar after! Register: docs.google.com/forms/d/1s9W...
@stearnslab.bsky.social @kelseymonson.bsky.social @rmassonix.bsky.social
Reposted by Neville Sanjana
matthewcobb.bsky.social
Whimsical footnote from my CRICK biography. Amber was a renowned mutation in a bacteriophage virus that stopped protein synthesis (so, “end of message” or “stop”). Its RNA codon is UAG.
Explanation of why it was called “amber” - a student who worked on the project was called Bernstein, which means “amber” in German.
nevillesanjana.bsky.social
What sad news… Sayan was such a wonderful human being. Thank you for sharing.
nevillesanjana.bsky.social
Amazing addition to @nygenome.org — very lucky to have a pioneer in functional genomics joining us.

Welcome Bing! 🚀🚀🚀
nygenome.org
We are proud to announce Bing Ren, PhD, as the new Scientific Director & CEO of the New York Genome Center

Dr. Ren brings his expertise in the fields of genomics & epigenetics to the NYGC & Columbia University, where he will hold a joint appointment.

For more on Dr. Ren: bit.ly/3DJXtah
Bing Ren Appointed Scientific Director and Chief Executive Officer of the New York Genome Center - March 27, 2025
Read about Bing Ren Appointed Scientific Director and Chief Executive Officer of the New York Genome Center at the New York Genome Center on March 27, 2025
bit.ly
nevillesanjana.bsky.social
Enjoyed participating in this far-ranging podcast about CRISPR and genome editing and its transformative impact on human health — and even more important in these challenging times.

www.thenakedscientists.com/podcasts/nak...
CRISPR, and the ethics of gene editing
The potential and the philosophy...
www.thenakedscientists.com
Reposted by Neville Sanjana
schvartzman.bsky.social
A patient reminded me of science’s power: 2 doses of immunotherapy and a fatal cancer GONE. Immunotherapy exists BECAUSE of basic research—work that can seem esoteric or wasteful. Before dismissing it, ask a scientist why it matters. Or ask the Nobel who discovered immunotherapy.
nevillesanjana.bsky.social
Thank you for following along and please check out the paper 📜 for more details.

The link in the first bleat (not skeet!) above is open-access. Also, you can find PDFs for this study and all others from our lab here: sanjanalab.org/papers.html
Sanjana Lab | papers
sanjanalab.org
nevillesanjana.bsky.social
I also want to highlight a similar study of the MYC locus in the context of different lymphomas (from
@russelljhryan.bsky.social & team), which has many complementary discoveries to our work: www.biorxiv.org/content/10.1...
nevillesanjana.bsky.social
Also I am very grateful to noncoding genomics funding from the MacMillan Center for the Study of the Noncoding Cancer Genome at NYGC, NHGRI and NCI. Without funding from these sources, this work would not have been possible.
nevillesanjana.bsky.social
Thanks also to co-authors @johnomix.bsky.social, Simon Müller, Alex Mendez-Mancilla, Evan Geller and Noa Liscovitch-Brauer. Many amazing labmates past and present contributed!
nevillesanjana.bsky.social
This study was led by a stellar team 💫: Staff scientist Christina Caragine and PhD student
Vicky Le. The idea for a "noncoding Cancer DepMap" started with some of my first students, Meer Mustafa and Bianca Diaz. Big shout-out to Meer & Bianca for their early contributions!
nevillesanjana.bsky.social
Given MYC's prime role in the progression of SO many different cancers, we hope these these tumor-specific regulators yield potential therapeutic targets for this “undruggable” oncogene. 💊 CRE discovery from saturation CRISPR screens presents an important step towards this ultimate goal.
nevillesanjana.bsky.social
In parallel with CREs from the CRISPR screen, we took an even broader approach: Using expression data from thousands of tumors and normal tissues, we found many TFs with cancer-specific MYC-correlated expression (>5-fold higher cancer vs. normal tissue).
nevillesanjana.bsky.social
Getting back to the MYC story, we next wondered whether the CREs we identified bind specific TFs. We looked for those TFs whose expression was correlated with MYC expression and where binding sites could be identified in the CREs.
nevillesanjana.bsky.social
As we showed recently in other work, the biology of essential noncoding RNAs is fascinating and more work is needed. Here's a link to our recent Cas13-based screen of long noncoding RNAs for those interested:
sanjanalab.org/reprints/Lia...
sanjanalab.org
nevillesanjana.bsky.social
There is likely a combination of effects on growth driven by both a genomic enhancer and ncRNA transcript since expressing the same ncRNA in trans partially (but not completely) rescues the phenotype!
nevillesanjana.bsky.social
Although CCAT1-MYC looping was the largest change upon CCAT1 transcript loss, this wasn’t just a local change: Many DNA contacts were impacted outside of the MYC TAD — on the same chromosome and genome-wide!
nevillesanjana.bsky.social
How could a lncRNA impact gene expression?
We found that loss of the CCAT1 transcript led to DNA conformation changes; the physical contact between the DNA was impacted by the RNA.
nevillesanjana.bsky.social
One of the CREs identified in 3 cell lines is located at the promoter for the lncRNA CCAT1 (we can’t escape lncRNAs these days...!)

We found that cell growth decreased when the DNA was silenced AND when the CCAT1 transcript was targeted using a RNA-targeting CRISPR (Cas13).
nevillesanjana.bsky.social
How are these CREs regulating MYC?
Using H3K27ac HiChIP we found that all but one of the CREs is in physical contact with the MYC promoter. ➰

However, contact 👉👈 is not enough for regulation: less than 10% of all contacts to the MYC promoter were identified as CREs.
nevillesanjana.bsky.social
We perturbed these CREs in 1 or 2 cell lines were the CRE is present (from the CRISPRi screens) and 1 where it wasn’t. Indeed, we see decreased cell growth and decreased MYC expression in the cell lines with the CRE and no change in cells lines without the CRE.
nevillesanjana.bsky.social
How do we know these CREs regulate MYC?
For 3 of these CREs, we further tested cell growth and MYC expression after CRISPR perturbation.
nevillesanjana.bsky.social
Even for CREs that were previously identified in human or mouse studies (mostly using large deletions), we were able to increase the resolution of the CRE boundaries. 🎛️🗺️ Up to 10,000-fold in one case!